Search

Background: Current tobacco treatment guidelines have established the efficacy of available interventions, but they do not provide detailed guidance for common implementation questions frequently faced in the clinic. An evidence-based guideline was created that addresses several pharmacotherapy-initiation questions that routinely confront treatment teams. Methods: Individuals with diverse expertise related to smoking cessation were empaneled to prioritize questions and outcomes important to clinicians. An evidence-synthesis team conducted systematic reviews, which informed recommendations to answer the questions. The GRADE (Grading of Recommendations, Assessment, Development, and Evaluation) approach was used to rate the certainty in the estimated effects and the strength of recommendations. Results: The guideline panel formulated five strong recommendations and two conditional recommendations regarding pharmacotherapy choices. Strong recommendations include using varenicline rather than a nicotine patch, using varenicline rather than bupropion, using varenicline rather than a nicotine patch in adults with a comorbid psychiatric condition, initiating varenicline in adults even if they are unready to quit, and using controller therapy for an extended treatment duration greater than 12 weeks. Conditional recommendations include combining a nicotine patch with varenicline rather than using varenicline alone and using varenicline rather than electronic cigarettes. Conclusions: Seven recommendations are provided, which represent simple practice changes that are likely to increase the effectiveness of tobacco-dependence pharmacotherapy.

Rationale: The tobacco harm reduction literature is replete with vague language, far-reaching claims, and unwarranted certainty. The American Thoracic Society has increasingly recognized the need for a framework for reliably making such claims. Evidence-based standards improving the scientific value and transparency of harm reduction claims are expected to improve their trustworthiness, clarity, and consistency. Methods: Experts from relevant American Thoracic Society committees identified key topic areas for discussion. Literature search strategy included English language articles across Medline, Google Scholar, and the Cochrane Collaborative databases, with expanded search terms including tobacco, addiction, smoking, cigarettes, nicotine, and harm reduction. Workgroup members synthesized their evidentiary summaries into a list of candidate topics suitable for inclusion in the final report. Breakout groups developed detailed content maps of each topic area, including points to be considered for suggested recommendations. Successive draft recommendations were modified using an iterative consensus process until unanimous approval was achieved. Patient representatives ensured the document’s relevance to the lay public. Results: Fifteen recommendations were identified, organized into four framework elements dealing with: estimating harm reduction among individuals, making claims on the basis of population impact, appropriately careful use of language, and ethical considerations in harm reduction. Discussion: This statement clarifies important principles guiding valid direct and inferential harm reduction claims. Ideals for effective communication with the lay public and attention to unique ethical concerns are also delineated. The authors call for formal systems of grading harm reduction evidence and regulatory assurances of longitudinal surveillance systems to document the impact of harm reduction policies.

Balancing population-based efforts to modify the social and environmental factors that promote tobacco dependence with efforts to improve the delivery of case-based treatments is necessary for realizing maximum reductions in the cost and consequences of the disease. Public health antismoking campaigns following the 1964 Surgeon General's report on the health risks of smoking have changed social norms, prevented initiation among youth, and promoted abstinence among the addicted. However, the rate of progress enjoyed to date is unlikely to continue into the coming decades, given that current annual unassisted cessation rates among prevalent smokers remains fairly low. With more than 1 billion patient interactions annually, there is an enormous unrealized capacity for health-care systems to have an effect on this problem. Clinicians report a perceived lack of reimbursement as a significant barrier to full integration of tobacco dependence into health care. A more complete understanding of the coding and documentation requirements for successful practice in this critically important area is a prerequisite to increasing engagement. This paper presents several case-based scenarios illustrating important practice management issues related to the treatment of tobacco dependence in health care.

Since the mid-20th century, the scientific community has substantially improved its understanding of the worldwide tobacco epidemic. Although significant progress has been made, the sheer enormity and scope of the global problem put it on track to take a billion lives this century. Curbing the epidemic will require maximizing the impact of proven tools as well as the development of new, breakthrough methods to help interrupt the spread of nicotine addiction and reduce the downstream morbidity.Members of the Tobacco Action Committee of the American Thoracic Society queried bibliographic databases, including Medline, Embase, and the Cochrane Collaborative, to identify primary sources and reviews relevant to the epidemic. Exploded search terms were used to identify evidence, including tobacco, addiction, smoking, cigarettes, nicotine, and smoking cessation. Evidence was consolidated into three thematic areas: (1) determinants of risk, (2) maternal-fetal exposure, and (3) current tobacco users. Expert panel consensus regarding current gaps in understanding and recommendations for future research priorities was generated through iterative discussion.Although much has been accomplished, significant gaps in understanding remain. Implementation often lags well behind insight. This report identifies a number of investigative opportunities for significantly reducing the toll of tobacco use, including: (1) the need for novel, nonlinear models of population-based disease control; (2) refinement of "real-world" models of clinical intervention in trial design; and (3) understanding of mechanisms by which intrauterine smoke exposure may lead to persistent, tobacco-related chronic disease.In the coming era of tobacco research, pooled talent from multiple disciplines will be required to further illuminate the complex social, environmental and biological codeterminants of tobacco dependence.

St. Helena Hospital launched the first US residential stop-smoking program, The St. Helena Center for a Smoke-Free Life, in 1969. This observational report describes the center's treatment outcome rate for using a patient-centered approach to the use of tobacco dependence medications and behavioral treatment for patients who participated in the program from January 1, 2005 through December 31, 2007. A total of 284 patients used long-acting (nicotine patch, bupropion, and varenicline) and/or short-acting medications (nicotine nasal spray, nicotine gum, nicotine lozenge, and nicotine oral inhaler) alone or in combination during treatment and after discharge. Seven patients chose to use no medications. Patients using nicotine patch received a mean ± SD dose of 33.3±15.7 mg of nicotine in 16 hours (range, 5-90 mg). The 12-month 7-day point prevalence smoking abstinence rate after participation in the intensive, 1-week, residential program was 57.0%. Recommendations are discussed for future research and for implementing aspects of the St. Helena program in other treatment settings.

BACKGROUND: This study evaluated the efficacy of bupropion for relapse prevention in smokers with and without a past history of major depressive disorder. Changes in depressive symptoms were also examined.

The aim of this study was to identify predictors of successful relapse prevention in smokers receiving long-term sustained-release bupropion. Smokers (N=784) who were interested in stopping smoking were enrolled in a 7-week, open-label bupropion phase. Abstinent subjects at the end of treatment and eligible to proceed (N=429) were randomized to active bupropion or placebo through Week 52 and then followed for an additional year. The best overall predictor of less relapse to smoking was assignment to active bupropion. In aggregate, the results indicate that bupropion can be prescribed to diverse populations of smokers with expected comparable results. There was a medication effect that was independent of any predictor except older age and those who gained no or minimal weight during the open-label phase. Predictors of successful relapse prevention included lower baseline smoking rates, a Fagerstrom Tolerance Questionnaire score of

Background: Recent data suggest that women smokers respond differently than men to cessation pharmacotherapies, particularly nicotine replacement therapy (NRT). Lower abstinence and higher relapse rates are often reported for women treated with NRT. Gender effects for those treated with non-nicotinic, bupropion-hydrochloride sustained release for relapse prevention have not been studied. Methods: Data from a multicenter relapse-prevention (RP) trial of bupropion (November 1995–June 1998) were analyzed for gender differences. Men and women smokers (N=784) were treated with open-label bupropion for 7 weeks. Those abstinent at Week 7 ( n =432) were enrolled in the double-blind relapse-prevention phase and randomized to placebo or continued bupropion for 45 additional weeks. Results: Differences in point-prevalence abstinence rates between men (61.8%) and women (55.6%) in open-label bupropion (Week 7) were not significant. In the RP-phase Week 52, continuous abstinence rates for men and women were 37.8% and 36.4% (bupropion) and 36.6% and 29.9% (placebo), respectively; point-prevalence abstinence rates for men and women were 54.1% and 55.9% (bupropion) and 42.9% and 41.3% (placebo), respectively. Abstinence rates and time to relapse were superior for both men and women who received longer treatment. Gender differences within treatment groups were not significant. Median time to relapse was equal for men and women within each treatment group: Week 32 for bupropion and Week 20 for placebo. Conclusions: Our data suggest that bupropion is a promising pharmacotherapy for preventing relapse, particularly for women.

Objectives: To identify predictors of smoking abstinence at the end of medication use that could assist in the optimal use of a sustained-release (SR) form of bupropion for treating cigarette smokers. Design: A double-blind, placebo-controlled, dose-response trial. Setting: Multicenter (three sites) study conducted in the United States. Participants: Six hundred fifteen healthy men and women (≥ 18 years of age) who were smoking ≥ 15 cigarettes per day and who were motivated to stop smoking. Intervention: Random assignment of patients to placebo or SR bupropion treatment, 100, 150, or 300 mg/d, for 7 weeks (total duration of study was 52 weeks: 7 weeks of treatment and 45 weeks of follow-up). Measurements and results: Logistic regression was used to identify predictors of abstinence at the end of the medication phase. Univariate predictors included the following: bupropion dose (p 4 weeks (p Conclusion: Bupropion SR therapy was effective in treating cigarette smokers independently of all other characteristics studied. Lower smoking rate, brief periods ( ie , ie , > 4 weeks) of abstinence with previous attempts to stop smoking, and male gender were predictive of better outcomes, independent of the dose of bupropion that was used.

A population pharmacokinetic and pharmacodynamic analysis evaluated the relationships of dose, plasma concentrations of bupropion and metabolites, and patient covariates with the safety and efficacy of bupropion sustained release (SR) for smoking cessation. A total of 519 outpatient chronic cigarette smokers were randomized to one of three bupropion SR doses: 100, 150, or 300 mg/day or placebo. The bupropion plasma concentration time data were fit and subject-specific bayesian estimates of clearance were obtained. Logistic regression analyses evaluated the role of dose, concentrations, and covariates in predicting efficacy and safety endpoints. For the evaluation of efficacy, patients were classified as quitters or non-quitters on the basis of a 4-week quit variable (defined as complete abstinence for weeks 4-7 of the study). For the evaluation of safety, patients were classified into two categories for each adverse event evaluated, corresponding to whether the patient ever experienced the adverse event during the course of the study or never experienced the event, regardless of whether the event was treatment-emergent. The efficacy of bupropion SR in facilitating smoking cessation was found to be related to dose and a mean metabolite concentration, and quitting in general was found to be related to the number of cigarettes smoked per day at baseline. Smoking cessation was 1.42, 1.69, and 2.84 times more likely in patients receiving 100, 150, and 300 mg/day of bupropion SR, respectively, as compared to placebo (p = 0.0001). As the baseline number of cigarettes smoked per day increased, the likelihood of quitting decreased regardless of the treatment condition. Insomnia and dry mouth were positively associated with mean metabolite concentrations, and dry mouth was inversely related to patient weight. Anxiety was inversely related to predicted steady-state concentration (Cpss), suggesting a positive effect on this withdrawal symptom. Bupropion SR exhibits a statistically significant dose/plasma level-response relationship for smoking cessation. Dry mouth and insomnia, related to concentrations, may be managed with dose reduction, with the realization that smoking cessation may be impaired.

Tobacco dependency syndrome is an organic disease caused by chronic use of inhaled tobacco smoke. It is occasionally controlled by willpower alone, but often requires pharmacotherapy in conjunction with various techniques to manage the psychological manifestations. The two effective drugs are bupropion, which is an oral antidepressant, and nicotine, which can be administered by several modalities, including a skin patch, an oral inhalant, a nasal spray, and a chewable oral preparation. Successful therapy may require both drugs, and multiple simultaneous nicotine modalities. High-dose nicotine therapy may achieve an abstinence rate of 80% during therapy, but maintaining drug-free abstinence at such high levels over long periods is less successful, possibly because the tobacco smoke-induced changes in brain structure and function are not easily reversed.

BackgroundA past history of major depression or alcoholism has been associated with poorer smoking treatment outcomes.AimTo evaluate the efficacy of bupropion for smoking cessation in smokers with a former history of major depression or alcoholism, and changes in depressive symptoms during smoking abstinence.MethodData were drawn from a multicentre trial of bupropion for smoking cessation. Smokers (n=615) received placebo or bupropion sustained-release at 100, 150, or 300 mg/day for six weeks after target quit date (TQD). The primary outcome was the point prevalence smoking abstinence at the end of treatment and at one year. The Beck Depression Inventory (BDI) was used to assess depressive symptoms.ResultsA significant dose – response effect of bupropion for smoking cessation was found. This was independent of history of major depression or alcoholism. Among those continuously abstinent from smoking for two weeks following TQD, an increase in BDI score was associated with a return to smoking at end of treatment.ConclusionsBupropion is efficacious for smoking cessation independently of a former history of major depression or alcoholism. Increases in depressive symptoms during an initial period of abstinence are associated with a return to smoking.

Trials of antidepressant medications for smoking cessation have had mixed results. We conducted a double-blind, placebo-controlled trial of a sustained-release form of bupropion for smoking cessation. We excluded smokers with current depression, but not those with a history of major depression. The 615 subjects were randomly assigned to receive placebo or bupropion at a dose of 100, 150, or 300 mg per day for seven weeks. The target quitting date (or "target quit date") was one week after the beginning of treatment. Brief counseling was provided at base line, weekly during treatment, and at 8, 12, 26, and 52 weeks. Self-reported abstinence was confirmed by a carbon monoxide concentration in expired air of 10 ppm or less.At the end of seven weeks of treatment, the rates of smoking cessation as confirmed by carbon monoxide measurements were 19.0 percent in the placebo group, 28.8 percent in the 100-mg group, 38.6 percent in the 150-mg group, and 44.2 percent in the 300-mg group (P0.001). At one year the respective rates were 12.4 percent, 19.6 percent, 22.9 percent, and 23.1 percent. The rates for the 150-mg group (P=0.02) and the 300-mg group (P=0.01) -- but not the 100-mg group (P=0.09) -- were significantly better than those for the placebo group. Among the subjects who were continuously abstinent through the end of treatment, the mean absolute weight gain was inversely associated with the dose (a gain of 2.9 kg in the placebo group, 2.3 kg in 100-mg and 150-mg groups, and 1.5 kg in the 300-mg group; P= 0.02). No effects of treatment were observed on depression scores as measured serially by the Beck Depression Inventory. Thirty-seven subjects stopped treatment prematurely because of adverse events; the frequency was similar among all groups.A sustained-release form of bupropion was effective for smoking cessation and was accompanied by reduced weight gain and minimal side effects. Many participants in all groups were smoking at one year.

Health professionals can effectively help patients quit smoking with a minimal, intervention-oriented, office-based treatment program. Clear-cut, unequivocal, unambiguous, stop-smoking advice can produce sustained, 1-year abstinence rates in the 5% range. This capability has been clearly documented for physicians. Dental literature increasingly supports the same conclusion for dentists. These studies show that although the yield from such brief advice may seem small, it is 17 times greater than the yield which results from saying nothing. Moreover, because dentists and physicians see so many patients during the course of 1 year, the potential impact of such intervention is staggering. More than 3.5 million patients could be cured of tobacco dependence annually. While specialized smoking cessation treatment programs can achieve 1 year sustained abstinence rates as high as 70%, they reach relatively few patients and can only achieve such high success rates because of the intensive, time-consuming nature of their interventions. The impact of basic dental advice can be increased during regular follow-up visits, when "teachable moments" in dental health often occur. Impact of advice on the 1-year sustained abstinence rates can be increased by arranging to see the patient at regular follow-up visits after the target quit date has been set, making certain that the medication, nicotine polacrilex, is used correctly.(ABSTRACT TRUNCATED AT 250 WORDS)

Although the use of over the counter (OTC) nicotine replacement therapy (NRT) is effective for smoking cessation, many concerns and misunderstandings persist that may reduce the effectiveness of NRT. Clinical practice and public health experts responded to a questionnaire that explored challenges associated with promoting proper NRT use and gathered recommendations on overcoming these challenges. Two predominant themes emerged including the identification of policies and practices that hinder NRT use, and smokers' views regarding NRT use. To address these needs, a two-part consensus statement about the use of OTC NRT to quit smoking was developed. The first part of the consensus statement identifies policy issues. The second part of the consensus statement was developed for smokers to reduce misperceptions and concerns about NRT by providing information on safety and the most effective use of NRT. The statement integrates state of the art clinical practice guidelines in a patient-centered format and presents information for policy makers to effectively support quit attempts.

Research has suggested that race, gender, and menthol cigarette use influence tobacco-smoke exposure measures and smoking-related disease risk. For example, a high proportion of Black smokers prefer menthol cigarettes and, despite smoking fewer cigarettes per day (CPD) than do Whites, tend to have higher cotinine levels. Additionally, Black males are more at risk for smoking-related lung cancer. High cotinine levels and smoking menthol cigarettes may lead to higher toxin intake, which contributes to increased disease risk. We explored the relationship between tobacco exposure variables (i.e., cotinine, CPD, carbon monoxide [CO], nicotine content, and nicotine dependence) with respect to race, gender, and menthol content in a sample of 307 smokers recruited from the greater Boston area to participate in a smoking cessation treatment trial. The pattern of correlations between tobacco exposure measures and cotinine showed a consistently positive correlation between cotinine and CO in all smokers and a correlation between cotinine and CPD in those who smoked nonmenthol cigarettes. Cotinine and CPD correlations varied by gender and race among menthol cigarette smokers. Consistently, we found a significant gender x race x menthol interaction on salivary cotinine level as well as cotinine/CPD ratio. These findings suggest that the relationship between number of cigarettes consumed and salivary cotinine is more complex than previously believed. It is not sufficient to look at race alone; researchers and clinicians need to look at race and gender concurrently, as well as type of cigarette consumed.

Objective To assess the efficacy of bupropion SR on smoking abstinence using a "slips allowed" analysis. Methods Retrospective analysis, which did not consider brief episodic "slips" as a return to regular smoking, of data from a multicenter, randomized, doubleblind, placebo-controlled relapse prevention study. Results Using a slips-allowed analysis, median time to relapse on bupropion SR was 65 weeks versus 30 weeks on placebo. This is compared to 32 and 20 weeks, respectively, using a traditional analysis not allowing for slips. Conclusion Bupropion SR is efficacious for the prevention of smoking relapse. A slips-allowed analysis may provide a more clinically relevant assessment of efficacy.

Background. This study was designed to test a dissemination model for providing clinical preventive medicine (CPM) training to general internal medicine faculty across the United States. Methods. The model incorporated direct instruction of a few faculty as seminar facilitators who, in turn, taught a CPM curriculum to their faculty colleagues, who then could teach it to housestaff and students. The CPM curriculum consisted of six seminars that focused primarily on the risk factors for chronic diseases and on behavior change methods for modifying smoking, diet, and exercise. Results. Faculty who participated in the seminars had significant pre- to post-test increase in knowledge and reported self-efficacy to implement CPM strategies with patients, as well as changes in CPM clinical practices. These faculty, in turn, successfully disseminated CPM information to their housestaff, who also had increases in self-efficacy and changed clinical practices regarding CPM topics. Conclusions. The successful implementation of the dissemination model attests to its viability as a mechanism for disseminating CPM curricula and increasing the emphasis on CPM issues in both clinical teaching and clinical encounters with patients.

Tobacco smoking has been irrefutably linked to lung cancer risk. Exposure to environmental tobacco smoke and lung cancer risk has been more controversial. Various sources have claimed confounding factors such as diet and classification bias could account for the reported link. We review the available evidence and some recent papers on this topic and conclude that the evidence linking environmental tobacco smoke and lung cancer is unequivocal and cannot be explained by confounding factors.

During the last 15 years substantial advances in the fields of analytical chemistry, behavioral pharmacology, neurologic sciences, and the behavioral sciences have produced new understanding and insight into why people smoke and how they can stop. These fundamental research efforts have now produced treatment strategies that have objectively documented success rates and that the physician can now implement in his office. Impressive as current results can be, when the physician is willing to spend appropriate and necessary time, effort, and energy, current research indicates that our basic neurochemical understanding of cigarette smoking should improve substantially and lead to even more effective treatment interventions in the next 10 years.

To assess the potential medical risks of rapid smoking, 24 healthy, male cigarette smokers were examined under the following conditions: baseline (after 12-hr tobacco abstinence), normal smoking, and rapid smoking. After normal and rapid smoking standard 12-lead EKG, arterial blood gases, and vital signs were evaluated, and during rapid smoking each subject was monitored electrocardiographically throughout the session. During or after rapid smoking there were no EKG abnormalities. Heart rate, respiratory rate, and systolic blood pressure rose after normal and rapid smoking. Many subjects developed elevated arterial pH with lowered serum potassium after rapid smoking, and two-thirds of the subjects developed relative hypoxemia. Among those who completed treatment, 61% were still abstaining from cigarettes after 6 months. Rapid smoking was found to be safe for healthy subjects. However, the safety of the technique among persons with cardiopulmonary disease cannot be predicted from the results of this study.

We studied 24 healthy young male smokers to ascertain the medical safety of a highly effective smoking-abatement technique called rapid smoking. In comparison with results obtained after a 12-h cigarette fast or after normal smoking, statistically significant increases occurred after rapid smoking in heart and respiratory rates, systolic blood pressure, carboxyhemoglobin, and pH (p less than 0.05), while arterial PCO2, HCO3-, and serum [K+] fell (p less than 0.05). Rapid smoking produced alveolar hyperventilation in all subjects. In eight, arterial PO2 increased appropriately, but in 16, fell paradoxically (p less than 0.01); seven had arterial PO2 below 80 torr. Because this fall could represent ventilation/perfusion mismatch due to early bronchoconstrictive disease, in subjects with normal flow/volume loops and spirometry rapid smoking may be a simple, provocative screening test for early airway disease. Despite the changes produced there were no arrhythmias. Rapid smoking is safe for healthy subjects but should not now be used for higher-risk patients.

Many occupational epidemiology studies require complete and accurate information on tobacco use to control for confounding by smoking and to assess interactions of smoking with workplace exposures. This paper reviews and evaluates the availability, reliability, validity, and efficiency of the various data sources and techniques for obtaining individual smoking data, including existing records, biological markers, and surveys. Emphasis is placed on the highly problematic issue of obtaining retrospective smoking histories. In general, the survey technique is currently deemed the most feasible approach for obtaining lifetime smoking histories. Both theoretical and practical aspects of smoking surveys are discussed in detail and are illustrated with a review of the recent literature and with data from two recent retrospective cohort studies conducted at the University of Pittsburgh. Several recommendations involving both the use of smoking data and areas for future methodologic research are presented. These include (1) justification for collecting smoking data in occupational studies based primarily on the potential for smoking to act as an effect modifier rather than solely as a confounder, (2) checks for reliability and validity in all studies which involve the collection of smoking data, (3) more methodologic research to better understand the impact that missing, unreliable, and invalid smoking data may have on the ability to detect and quantify important smoking-exposure interactions, and (4) an assessment of the correlation between biological markers and cigarette carcinogen exposure.

Nicotine polacrilex (Nicorette) is the only medication approved by the Food and Drug Administration for tobacco dependency treatment. It is available only by prescription. This study sought to determine whether this medication produced any adverse gingival effects. Thirty-one patients (91%) used the nicotine polacrilex for at least 1 month and 20 (59%) for 3 months or more. Five (15%) developed small (less than 2 mm), painless, clear, nonhemorrhagic vesicles which resolved immediately when patients were reinstructed to position the medication in different sites in the mouth. There were no changes in gingival color, contour, consistency and texture, tooth mobility, or periodontal pocket depth. Nicotine polacrilex does not appear to have any significant adverse effects on the gingiva even with up to 6 months of daily use.

Patients with systemic necrotizing vasculitis frequently present as diagnostic dilemmas. In previous series of patients with polyarteritis nodosa, less than one third were diagnosed antemortem. Although current clinical awareness of systemic necrotizing vasculitis is greater than in the past and procedures for the diagnosis of these diseases have improved, patients commonly present with atypical features. The diagnosis of a systemic necrotizing vasculitis frequently remains unsuspected or unproven until an involved tissue is biopsied. We report an unusual case of systemic necrotizing vasculitis in which the diagnosis was confirmed by a transbronchial biopsy of the lung which demonstrated pulmonary capillaritis with hemorrhage.